V Test 1 Kuma (Dlp)

Front 1

po Dose recommendations for Bumetanide in Chronic Heart Failure

Back 1

* Initial: 0.5 to 1 mg qd or bid * Maximum total daily dose: 10 mg

Front 2

po Dose recommendations for Furosemide in Chronic Heart Failure

Back 2

* Initial: 20 to 40 mg qd or bid *Maximum total daily dose: 600 mg

Front 3

po Dose recommendations for Torsemide in Chronic Heart Failure

Back 3

* Initial: 10 to 20 mg qd * Maximum total daily dose: 200 mg

Front 4

IV Dose recommendations for Bumetanide in Severe Heart Failure

Back 4

* Initial: 1 mg *Maximum single dose: 4 to 8 mg

Front 5

IV Dose recommendations for Furosemide in Severe Heart Failure

Back 5

* Initial: 40 mg * Maximum single dose: 160 to 200 mg

Front 6

IV Dose recommendations for Torsemide in Severe Heart Failure

Back 6

* Initial: 10 mg *Maximum single dose: 100 to 200 mg

Front 7

When do you initiate conintuous IV infusion of a loop diuretic?

Back 7

When you have reached the MAX single IV dose and the patient still has edema

Front 8

po Dose recommendations for Metolazone (for sequential nephron blockade) in Chronic Heart Failure

Back 8

2.5 to 10 mg qd plus a loop diuretic

Front 9

po Dose recommendations for Chlorothiazide IV (for sequential nephron blockade) in Chronic Heart Failure

Back 9

250 to 500 mg qd or bid plus a loop diuretic

Front 10

po Dose recommendations for Hydrochlorothiazide (for sequential nephron blockade) in Chronic Heart Failure

Back 10

12.5 to 25 mg qd or bid plus a loop diuretic

Front 11

po Dose recommendations for Chlorothiazide IV (for sequential nephron blockade) in Severe Heart Failure

Back 11

250 to 1000 mg IV once or twice plus a loop diuretic once

Front 12

Convert po Furosemide 80 mg to IV Furosemide

Back 12

40 mg Furosemide IV (when going from po to IV cut the dose in half)

Front 13

Convert IV Furosemide 80 mg to po Furosmide

Back 13

160 mg Furosemide po (when going from IV to po double the dose)

Front 14

Convert from 5 mg Bumetanide po to Furosemide po

Back 14

200 mg Furosemide po (the "exchange rate" is 1 mg Bumetanide to 40 mg Furosemide)

Front 15

Convert from 80 mg Furosemide po to Torsemide po

Back 15

40 mg Torsemide po (the "exchange rate" is 20 mg Furosemide to 10 mg Torsemide)

Front 16

Convert from 5 mg Bumetanide IV to Bumetanide po

Back 16

5 mg Bumetanide po (Bumetanide is 100% bioavailable po)

Front 17

Convert from 100 mg Torsemide po to Torsemide IV

Back 17

100 mg Torsemide IV (Torsemide is 100% bioavailable po)

Front 18

What is the major role of loop diuretics in HF?

Back 18

decrease plasma volume

Front 19

What are the effects of loop diuretics on mortality?

Back 19

no improvement in outcomes

Front 20

What are the side effects associated with loop diuretics?

Back 20

decreased levels of Mg, K, Ca, aotemia, metabolic alkalosis

Front 21

What is the risk of a K level below 4 or above 5.5?

Back 21

increased risk of arrhythmias

Front 22

What monitoring is necessary when administering a loop diuretic?

Back 22

* Chem-7, mental status, input/output, weight, edema * Inpatient: daily * Outpatient: weight daily at home, electrolytes q2wks x 1 month, then monthly

Front 23

What is the effect of Hydralazine?

Back 23

arterial vasodilation which leads to a decrease in afterload

Front 24

What are doses for Hydralazine?

Back 24

*Initial: 10 to 25 mg Hydralazine po TID to QID * MAX: 75 mg po TID to QID

Front 25

What side effects are associated with Hydralazine?

Back 25

drug induced Systemic Lupus Erythematosus (15%)

Front 26

What is the effect of Isosorbide Dinitrate (ISDN)?

Back 26

venous vasodilation which leads to a decrease in preload

Front 27

What are the recommended doses for Isosorbide Dinitrate (ISDN)?

Back 27

10-40 mg Isosorbide Dinitrate po TID

Front 28

What are the side effects associated with Isosorbide Dinitrate (ISDN)?

Back 28

hypotension, headache, dizziness

Front 29

What are the side effects associated with Hydralazine/Isosorbide Dinitrate combination therapy?

Back 29

Headache (19% of patients may not tolerate)

Front 30

What is the effect of Angiotensin II on Vascular smooth muscle?

Back 30

increased arteriolar constriction leading to increased arterial blood pressure

Front 31

What is the effect of Angiotensin II on Central & peripheral nervous system?

Back 31

facilitation of sympathetic activity which leads to increased arteriolar constriction and increased cardiac output leading to increased arterial blood pressure

Front 32

What is the effect of Angiotensin II on the adrenal cortex?

Back 32

increased aldosterone secretion which leads to increased Na resorption leading to increased arterial blood pressure

Front 33

What is the effect of Angiotensin II on the kidney directly?

Back 33

* in the tubules: increased Na resorption leading to increased arterial blood pressure * In the arterioles: increased filtration fraction leading to increased Na resorption leading to increased arterial blood pressure and decreased GFR leading to Na and H2O retention leading to increased arterial blood pressure

Front 34

What is the effect of Angiotensin II on the brain?

Back 34

increased ADH leading to increased H2O resorption, Na and H2O retention leading to increased arterial blood pressure AND increased thirst leading to increased H2O ingenstion, Na and H2O retention leading to increased arterial blood pressure

Front 35

What are the recommended doses for Captopril?

Back 35

* Initial: 6.25 mg TID *MAX: 50 mg TID

Front 36

What is a benefit of Captopril?

Back 36

It is short acting so you can initiate a patient on a "challenge" starting at 6.25 mg TID then 12.5 TID, then 25 mg TID then switch to another agent

Front 37

What are the recommended doses for Enalapril?

Back 37

* Initial 2.5 mg BID *MAX: 10 to 20 mg bid

Front 38

What are that recommended doses for Lisinopril?

Back 38

* Initial 2.5 to 5 mg qd *MAX: 20 to 40 mg qd

Front 39

What is the MOA of ACE inhibitors?

Back 39

inhibit the angiotensin converting enzyme leading a decrease in angiotensin II and inhibit the breakdown of Bradykinin leading to an increase in Bradykinin

Front 40

What are the patient considerations with ACE inhibitors?

Back 40

1. Adherance b/c this drug is a life saver

2. Side effects: Dry cough, renal dysfunction, hyperkalemia, angioedema, neutropenia, hypotension

3. Monitoring: Chem-7 with Mg and CA q2wks x 1 month then monthly, CBC monthly, BP q2wks x1 month then monthly (timelines are outpatient - inpatient all are checked daily)

4. Drug interactions: Lithium, NSAIDS, Salt subs, Loop diuretics, K sparing diuretics

5. Contraindications: Pregnancy, Hx of angioedema, renal artery stenosis, hyperkalemia

Front 41

Benefits to using an ACE inhibitor?

Back 41

* Reduce all cause mortality, reduce mortality related to HF, reduce hospitalizations for HF, improve overall symptoms

* Greater benefit with worsening HF 10-60% with class I benefiting ~10% and class IV benefiting ~60%

* Prevent new onset DM and HF

* No difference in all cause mortality between high vs. low doses. Using a lower dose allows you to get more drugs on board with the patient.

Front 42

What is the MOA of ARBs?

Back 42

Blocks the Angiotensin II receptor which bypasses non-renin and non-ACE pathways to decrease Angiotensin II

Front 43

What are the recommended doses for Candesartan?

Back 43

* Initial: 4 to 8 mg qd * MAX: 32 mg qd

Front 44

What are the recommended doses for Losartan?

Back 44

* Initial: 25 to 50 mg qd * MAX: 50 to 100 mg qd

Front 45

What are the recommended doses for Valsartan?

Back 45

* Initial: 20 to 40 mg bid * MAX: 160 mg bid

Front 46

What are the patient considerations for ARBs?

Back 46

1. Adherance - keep appointments 2. Side effects: well tolerated with less angioedema than ACEi's, hyperkalemia, uricosuric effects, renal dysfunction, neutropenia 3. Drug interactions: not listed 4. Precautions/Contraindications: overproducers of uric acid, pregnancy, volume depletion, renal artery stenosis

Front 47

What are the benefits of using an ARB?

Back 47

* At least as effective as an ACEi in reducing all cause mortality, suddeen death, and hospitalization * Can prevent new onset DM

Front 48

What are the effects of Digoxin?

Back 48

* Resets the baroreceptors, inotropic effects, switches off the sympathetic response and turns on the parasympathetic nervous system

Front 49

What are the optimal serum concentrations for Digoxin?

Back 49

0.5 to 0.8 mcg/L serum concentrations over 1.2 mcg/L are toxic

Front 50

What are the monitoring parameters for Digoxin?

Back 50

Serum concentrations and Electrolytes: Mg, Ca, K, BUN, Scr…Especially K and Scr

Front 51

What are signs of Digoxin toxicity?

Back 51

N/V, anorexia, bradycardia, heart block, green halos

Front 52

What drug interactions with Digoxin?

Back 52

Propafenone, Qunidine, Amiodarone, Macrolides (Erythromycin and Clarythromycin. Inducers: St Johns Wart and Rifampin (cut dose by 50%)

Front 53

What are the benefits of using Digoxin?

Back 53

No effect on all cause mortality, but does decrease hospitalization for worsening HF, reduced combination of hospitalization and death via HF but with high risk of arrhythmias

Front 54

Are patients usually taken off Digoxin one it has been started?

Back 54

removal of Digoxin increases the risk for HF exacerbation

Front 55

Is there an increased risk of death in women vs men?

Back 55

Once serum concentrations were looked at more closely, it was found that there is no sex related difference in Dig mortality

Front 56

What are the beneficial effects of Beta blockers?

Back 56

Block the down regulation of beta1 receptors, inhibit apoptosis/oxidative stress, decreased arrhythmia potential, and inhibit hypertrophy/fibrosis (think of Beta blockers as a shield blocking the heart from the negative effects of NE)

Front 57

What are the three classes of Beta blockers?

Back 57

* First generation are non-selective beta blockers - Propranolol, Nadolo, and Timolol (not used in HF) * Second generation are Beta1 selective beta blockers - Atenolol, Bisoprolol, and Metoprolol/Metoprolol XL * Third generation beta blockers have other benefits like alpha inhibition or glycoprotein effects - Bucindolol, Carvedolol, and Labetolol

Front 58

What three beta blockers are most often used in HF?

Back 58

Bisoprolol, Carvedilol, and Metroprolol XR

Front 59

What are the recommended doses of Bisoprolol?

Back 59

* Initial: 1.25 mg qd * MAX: 10 mg qd

Front 60

What are the recommended doses of Carvedilol?

Back 60

* Initial: 3.125 mg bid * MAX: 25 mg bid

Front 61

What are the recommended doses of Metoprolol XR?

Back 61

* Initial: 12.5 to 25 mg qd *MAX: 200 mg qd

Front 62

Which patients are appropriate candidates for Beta blocker therapy?

Back 62

* Mild or moderate symptoms of HF (classes II, III, and class IV if stable, not on IV drugs) *Systolic dysfunction of the left ventricle (EF <40%) * Receiving treatment with an ACE inhibitor and a diuretic *Any age and either sex * CAD or nonischemic dilated cardiomyopathy * Diabetic and nondiabetic * COPD without reactive airway disease

Front 63

When should treatment with a beta blocker be ideally started?

Back 63

* Tx with a diuretic so that the patient has minimal evidence of fluid retention * Tx with an ACE inhibitors *No recent use of IV vasodilators or positive inotropic agents * Systolic bloop pressure > or = 90 mmHg * HR > 60 BPM (unless tx with pacemaker)

Front 64

List patient education points for beta blocker therapy.

Back 64

* Tell patients that they are going to feel like crap for the first 3 months then they are going to feel like a million bucks (crap phase is from coming down off the CCAs) * Patient needs to weigh themselves 2-3 times daily and call in if they gain 2-3 lbs * Call immediately if any signs of SOB, edema, bradycardia, or weight gain * Never stop the beta blocker unless the patient has 3rd degree heart block or is in cardiogenic shock - cut dose in half if needed

Front 65

Which should be started first an ACEi or a beta blocker?

Back 65

This is a point of controversy but the ACEi and diuretic should still be started first

Front 66

If both and ACEi and a beta blocker are on board, which one do you increase the dose on first?

Back 66

Always increase the beta blocker to the highest possible dose to have the most decrease risk of mortality

Front 67

What are the effects of Aldosterone in HF?

Back 67

* Mg/K loss leading to QT dispersion and ventricular arrhythmias leading to cardiac death * Sympathetic activation leading to tachycardia ischemia leading to QT dispersion and ventricular arrhythmias leading to cardiac death * Parasympathetic inhibition leading to Tachycardia ischemia leading to QT dispersion and ventricular arrhythmias leading to cardiac death * Myocardial fibrosis leading to QT dispersion and ventricular arrhythmias leading to cardiac death

Front 68

What are the effects of Aldosterone on the body?

Back 68

* Heart - Myocardial fibrosis, ventricular arrhythmias, left ventricular hypertrophy * Vasculature - HTN, fibrosis, endothelial dysfunction, inhibits NO synthesis, prothrombotic * Kidney - Na retention and K/Mg loss * CNS - increased Catecholamines

Front 69

What are the dosing recommendations for spironolactone?

Back 69

* Initial: 12.5 to 25 mg qd *MAX: 25 mg qd or bid

Front 70

What are the dosing recommendations for Eplerenone?

Back 70

* Initial: 25 mg qd * MAX: 50 mg daily

Front 71

What side effects does Spironolactone have that Eplerenone does not?

Back 71

Gynecomastia (10 to 15%)and errectile dysfunction because Spirononlactone blocks the Androgen receptors while Eplerenone only block the Mineralocorticoid receptors

Front 72

What are the benefits of Spironolactone?

Back 72

In class III to IV patients: reduction in CV & HF mortality, sudden death, CV & HF hospitalization

Front 73

What are the benefits of Eplerenone?

Back 73

In class I-II post MI patients: reduction in all cause mortality, sudden death, and death from CV mortality or hospitalization

Front 74

Steps to Minimize hyperkalemia

Back 74

1.  Impaired renal function is a risk factor for hyperkalemia during treatment with aldosterone antagonists. This risk increased progressively when Scr exceeds 1.6 mg/dL. ClCr > 30 mL/min is recommended. 2. Aldosterone antagonists should not be administered to patients with baseline serum K > 5.0 mEq/L 3. Intial doses of spironolactone 12.5 mg or eplerenone 25 mg is recommended, then the dose can be increased to spironolactone 25 mg or eplerenone 50 mg if appropriate 4. Risk of hyperkalemia is increased with concomitant use of higher doses of ACEi’s (captopril 75 mg qd or more, emalapril or Lisinopril 10 mg qd or more) – Minimize the ACEi dose 5. NSAIDS and COX-2 inhibitors should be avoided 6. K supplements should be reduced or discontinued 7. Close monitoring of serum K is required. K levels and renal function should be checked in 3 days and at 1 week after initiation of therapy and at least monthly for 3 months. FOLLOW this schedule or don’t use 8. Diarrhea or other causes of dehydration should be addresses emergently

Front 75

What other agents can be used in HF?

Back 75

* Dihydropyridine CCBs - amolodipine, fenlodipine * Warfarin with an INR of 2-3 this is debateable *Amiodarone - used in atrial fibrillation * Statins - reduce hospitalizations independent of LDL * Hydralazine-ISDN 20 mg/37.5 mg TID especially in African Americans

Front 76

Why focus on African American patients?

Back 76

HF effects ~ 3% of the African American population, Occurs at an earlier age, Disease severity is more advanced, and African Americans have a higher rate of hospitalization & 1.8 x higher mortality rate, NO deficiency, TGFB mRNA, decreased role of RRA and increased endothelin-1

Front 77

What are the benefits of using Hydralazine-ISDN 20 mg/37.5 mg TID in the african american population?

Back 77

* decrease in mortality (30%), improved quality of life, and prolongs the time before the first time hospitalization for HF

Front 78

Can Hydralazine-ISDN replace an ACEi or beta blocker in the african american population?

Back 78

NO

Front 79

When should treatment with Hydralazine-ISDN be started?

Back 79

First ACEi/diuretic, then Beta blocker, then Digoxin, then Hydralazine-ISDN

Front 80

A 75 year old male with EF of 25% is receiving the following medications: Lisinopril 2.5 mg qd, ASA 81 mg qd, Digoxin 0.125 mg qd, Furosemide 40 mg bid, Carvedilol 12.5 mg qd, and Spironolactone 25 mg qd. His BP is 120/70 mmHg, Dig level is 0.8 ng/mL, and Scr of 1.3 mg/dL. Which of the following therapeutic strategies could furthur improve his outcomes (i.e. mortality)? A. Increase Lisinopril to 20 mg qd B. Increase Carvedilol to 25 mg bid C. Increase Furosemide to 80 mg bid D. Increase Digoxin to acheive a serum concentration of 1.5 ng/mL

Back 80

B. Increase Carvedilol to 25 mg bid

Front 81

How are Stage A patients managed?

Back 81

Goals: Treat HTN, Smoking sessation, treat hyperlipedemia, encourage exercise, Discourage alcohol intake and illicit drug use, Control metabolic syndrome * Drugs: Antiplatelet - ASA 81 mg - 325 mg or Plavix (clopidegrel), AntiHTN - ACEi or ARB, Lipid control - Statins for anti-inflammatory benefits above and beyond LDL control (Goal is LDL <70)

Front 82

How are Stage B and Stage C patients managed?

Back 82

Goals: Treat HTN, Smoking sessation, treat hyperlipedemia, encourage exercise, Discourage alcohol intake and illicit drug use, Control metabolic syndrome Drugs: 1) ACEi plus a loop diuretic (if patient does not tolerate ACEi, then use and ARB or Hydralazine/ISDN) 2) add a Beta blocker 3) If still s/s add Digoxin 4)If still s/s add aldosterone antagonist &/or ARB